ArticleDNA repair2015
Suppression of oxidative phosphorylation in mouse embryonic fibroblast cells deficient in apurinic/apyrimidinic endonuclease.
Article in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Mitochondrial DNA Damage and Histological Features in Liver Tissue of Azoxymethane-TreatedBiomolecules · 2025Article
- UC MSCs Educated Tenon (METn) Stimulates Tendon Regeneration Through Rejuvenation of the Complex and Tendon-Derived Cells (TDCs).Stem cells international · 2025Article
- A Novel HypomorphicAntioxidants & redox signaling · 2023Article
- Evaluation of antioxidant network proteins as novel prognostic biomarkers for head and neck cancer patients.Oral oncology · 2020Article
- Tumor-associated APE1 variant exhibits reduced complementation efficiency but does not promote cancer cell phenotypes.Environmental and molecular mutagenesis · 2017Article
- Polyubiquitination of apurinic/apyrimidinic endonuclease 1 by Parkin.Molecular carcinogenesis · 2017Article
- Neil2-null Mice Accumulate Oxidized DNA Bases in the Transcriptionally Active Sequences of the Genome and Are Susceptible to Innate Inflammation.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The mammalian apurinic/apyrimidinic (AP) endonuclease 1 (APE1) is an essential DNA repair/gene regulatory protein. Decrease of APE1 in cells by inducible shRNA knockdown or by conditional gene knockout caused apoptosis. Here we succeeded in establishing a unique mouse embryonic fibroblast (MEF) line expressing APE1 at a level far lower than those achieved with shRNA knockdown. The cells, named MEF(la) (MEF(lowAPE1)), were hypersensitive to methyl methanesulfonate (MMS), and showed little activity for repairing AP-sites and MMS induced DNA damage. While these results were consistent with the essential role of APE1 in repair of AP sites, the MEF(la) cells grew normally and the basal activation of poly(ADP-ribose) polymerases in MEF(la) was lower than that in the wild-type MEF (MEF(wt)), indicating the low DNA damage stress in MEF(la) under the normal growth condition. Oxidative phosphorylation activity in MEF(la) was lower than in MEF(wt), while the glycolysis rates in MEF(la) were higher than in MEF(wt). In addition, we observed decreased intracellular oxidative stress in MEF(la). These results suggest that cells with low APE1 reversibly suppress mitochondrial respiration and thereby reduce DNA damage stress and increases the cell viability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.